ライフサイエンスコーパス: PPADS

1 PPADS (100 microM) and suramin (300 microM) reduced the

2 PPADS [pyridoxal phosphate-6-azo(benzene-2,4-disulfonic

3 PPADS abolished this post-contraction increase in discha

4 PPADS and 2',3'-O-(2,4,6-trinitrophenyl)-ATP blocked alp

5 PPADS and suramin also reduced contractions to exogenous

6 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) (0.1-100 microM) and suramin (1-300 microM) inhib

7 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) at 10 microm.

8 hosphate-6-azo (benzene-2,4-disulfonic acid (PPADS) but not by the 5-HT3 antagonist tropisetron or th

9 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) was given.

10 l phosphate-6-azophenyl-2,4-disulfonic acid (PPADS), a P2X antagonist, attenuated the responses of gr

11 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), and more potently activated by 3'-O-(4-benzoyl)b

12 phosphate-6-azophenyl-2',5'-disulfonic acid (PPADS), pyridoxal-5'-phosphate-6(2'-naphthylazo-6-nitro-

13 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS).

14 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 10 micromol/L) reduced the control fEPSP amplitud

15 hosphate-6-azophenyl-2', 4'-disulfonic acid (PPADS; 20 microm).

16 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS; 50 mum) or suramin (150 mum) were added to the ex

17 phosphate-6-azophenyl-2',4' disulfonic acid (PPADS; a P(2X)-purinoceptor antagonist; 3 x 10(-5) mol/L

18 osphate-6-azophenyl-,2',4'-disulphonic acid (PPADS) and Mg2+ produced concentration-dependent inhibit

19 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), blocking Ca(2)(+)-dependent exocytosis from neur

20 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS).

21 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microM) or alpha,beta-methylene ATP (50-100 mi

22 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microm), reduced constrictions in MA but not i

23 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microM).

24 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 100 microM).

25 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 10 microM) or an NK(3) tachykinin receptor antago

26 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 100 microM), but not the adenosine receptor antag

27 ent apyrase, the purinergic receptor agonist PPADS, the calcium chelator BAPTA-AM, and calpain inhibi

28 is-1,3,5-na phthalene-trisulphonic acid) and PPADS (pyridoxal phosphate-6-azophenyl-2',4'-disulphonic

29 cotinic cholinergic receptor antagonist) and PPADS (P2X receptor antagonist).

30 , was a less effective agonist than ATP, and PPADS was a more potent inhibitor of the AcP2X receptors

31 We found that both OxATP and PPADS significantly improved functional recovery and dim

32 ion molecule-1 (ICAM-1), whereas suramin and PPADS decreased both ATPgammaS-induced and basal ICAM-1

33 Suramin and PPADS often reduced ongoing activity, and blocked the ex

34 by ivermectin but insensitive to suramin and PPADS, and it permeated the large cation N-methyl-d-gluc

35 Suramin and PPADS, general P2Y receptor blockers, and MRS2578, an in

36 ivity to the antagonists NF449, suramin, and PPADS was conferred by the nature of the extracellular l

37 uramin (14 micromol (kg body wt)-1 i.v.) and PPADS (17 micromol (kg body wt)-1 i.v.) antagonized the

38 The nonselective P2 antagonist PPADS or the P2Y1-selective antagonist MRS2179 failed to

39 d 2MeS-ATP mimics, while the P2XR antagonist PPADS blocks, the observed enhancement of the frequency

40 administration of the purinergic antagonist PPADS (1 or 3 mug kg(-1)).

41 this response by the P2 receptor antagonist PPADS suggests that bradykinin-induced micturition facil

42 pyrase or the purinergic receptor antagonist PPADS.

43 The P2X receptor antagonist, PPADS, nearly abolished the contractions.

44 d in the presence of P2 receptor antagonists PPADS (10 microm) and suramin (5 microm).

45 eceptors with the broad-spectrum antagonists PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate

46 ed by non-specific P2X receptor antagonists, PPADS or suramin.

47 ere partially attenuated by 1 mm suramin but PPADS (80 microm) had no effect.

48 The effects were attenuated by PPADS, an antagonist to P2X receptors.

49 ation of NMDA-evoked currents was blocked by PPADS (10 uM) and by chelation of intracellular Ca(2+) w

50 (ED50 22 +/- 5 nmol) and this was blocked by PPADS (17 micromol (kg body wt)-1 i.v.); unidentified va

51 sEPSC facilitation was blocked by PPADS (30 microm) and the selective P2X(3) receptor anta

52 ied in Ca2+/Mg2+-free medium, and blocked by PPADS or oxidized ATP.

53 The effect was blocked by PPADS, a protein kinase C inhibitor (bisindolylmaleimide

54 iring activity, effects that were blocked by PPADS.

55 n-dependently (1-30 micromol/L) inhibited by PPADS (50%-inhibitory concentration, 3 micromol/L).

56 in the holding current that was prevented by PPADS or kynurenic acid treatment, suggesting that ATP e

57 neurons from P2X2-/- mice were unaffected by PPADS but were blocked by mecamylamine.

58 /- 9 nmol), an action that was unaffected by PPADS or suramin.

59 he 6-azophenyl-2',4'-disulfonate derivative (PPADS), in which the phosphate group was cyclized by est

60 xal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS), 2'-deoxy-N6-methyladenosine 3',5'-bisphosphate (

61 xal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS), and to a lesser degree the nonspecific ectonucle

62 xal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS, a P2 receptor blocker) decreased the ventilatory

63 H)) ZD7288, or by the purinoceptor inhibitor PPADS.

64 the P2 receptor antagonists suramin and iso-PPADS.

65 inhibitor), P2X-purinoceptor antagonist (iso-PPADS), or genetic TRPV4 deficiency on hippocampal dopam

66 Intratracheal lidocaine, iso-PPADS, and TRPV4 genetic deficiency protected mice again

67 wer than PPADS (IC50 98.5 +/- 5.5 nM) or iso-PPADS (IC50 42.5 +/- 17.5 nM), although unlike PPADS its

68 Likewise, PPADS abolished the group IV afferent responses to stati

69 c receptor antagonists suramin (100 microm), PPADS (20-50 microm), and apyrase (80 U/ml), in contrast

70 now tested the hypothesis that injection of PPADS (10 mg kg(-1)) attenuated the responses of group I

71 Previously we have shown that injection of PPADS, a P2 receptor antagonist, into the arterial suppl

72 Suramin (200 microM) or PPADS (200 microM) applied by intra-arterial perfusion e

73 he P2 receptor agonists suramin (150 mum) or PPADS (50 mum) but were blocked by the connexin channel

74 CI), we delivered P2X7R antagonists OxATP or PPADS to rats after acute impact injury.

75 1,3-benzenedisulfonic acid tetrasodium salt (PPADS) (10 uM) or kynurenic acid (1 mm).

76 nyl-2',4'-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the reflex bradycardia (by app

77 ors or by purinoceptor antagonists (suramin, PPADS), and were essentially eliminated by blocking syna

78 or (IC50 10.2 +/- 2.6 microM) was lower than PPADS (IC50 98.5 +/- 5.5 nM) or iso-PPADS (IC50 42.5 +/-

79 In the present study, we found that PPADS attenuated the group III afferent responses to sta

80 ADS (IC50 42.5 +/- 17.5 nM), although unlike PPADS its effect was reversible with washout and surmoun

81 bited the peak amplitude of the IJP, whereas PPADS had no effect.

82 lunted by blocking purinergic receptors with PPADS (0.1-1 mM; intravesically).